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Titolo:
Yin6, a fission yeast Int6 homolog, complexes with Moe1 and plays a role in chromosome segregation
Autore:
Yen, HCS; Chang, EC;
Indirizzi:
NYU, Dept Biol, New York, NY 10003 USA NYU New York NY USA 10003NYU, Dept Biol, New York, NY 10003 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 26, volume: 97, anno: 2000,
pagine: 14370 - 14375
SICI:
0027-8424(200012)97:26<14370:YAFYIH>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAMMARY-TUMOR VIRUS; SCHIZOSACCHAROMYCES-POMBE; SPINDLE FORMATION; S-POMBE; GENE; RAS; MUTATIONS; PROTEINS; TUBULIN; GENOME;
Keywords:
signal transduction; C proteins; eukaryotic initiation factor 3; cell cycle; mouse mammary tumor virus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Chang, EC NYU, Dept Biol, 100 Washington Sq E, New York, NY 10003 USA NYU 100 Washington Sq E New York NY USA 10003 York, NY 10003 USA
Citazione:
H.C.S. Yen e E.C. Chang, "Yin6, a fission yeast Int6 homolog, complexes with Moe1 and plays a role in chromosome segregation", P NAS US, 97(26), 2000, pp. 14370-14375

Abstract

The INT6 gene has been implicated in human breast cancer formation, but its function is unknown. We isolated an Int6 homolog from fission yeast, Yin6by its binding to a conserved protein in the Ras pathway, Moe1. Yin6 and Moe1 converge on the same protein complex to promote microtubule instability/disassembly. Yin6 and Moe1 interact cooperatively: when either protein is absent, the other becomes mislocalized with decreased protein levels. Furthermore, whereas full-length human Int6 rescues the phenotypes of the yin6-null (yin6 Delta) mutant cells and binds human Moe1, truncated Int6 proteinsfound in tumors do not Importantly, yin6 Delta alone impairs chromosome segregation weakly, but yin6 Delta together with ras1 Delta causes severe chromosome missegregation. These data support a model in which INT6 mutations in humans either alone or together with additional mutations, such as a RASmutation, may contribute to tumorigenesis by altering genome stability.

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Documento generato il 01/12/20 alle ore 06:46:51